[Treatment of cyanide compound with ultraviolet radiation in waste fluid cotainting cyanmethemoglobin (II) (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Fujiwara.
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Further studies were carried out to investigate cellular sites of the resistance to the induction of immunological tolerance to HGG in DDD mice, assuming the presence of a subset of tolerogen-resistant splenic T cells. Spleen-seeking T cells were shown to be relatively resistant in comparison with lymph node-seeking T cells. The existence of a tolerogen-resistant T-cell subpopulation was indicated from the experiments demonstrating that tolerance was easily attained after adult thymectomy and that lymph node T cells became much more resistant to tolerance induction after adult splenectomy. The latter experimental result might also exclude the possibility of differences in microenvironment (probably in A cells) between spleen and lymph node. An attempt was made to investigate a possible involvement of A cells in the induction of tolerance. A cells were deprived in vivo by irradiation of the host 3 days prior to spleen cell transfer and in vitro by passing a spleen cell suspension through a Sephadox G-10 column. The deprivation of A cells resulted in priming of the host by the tolerogen rather than easier tolerance induction. No suppressive activity was observed in lymph node cells from tolerized mice. These results suggest that there exists a set of T cells, generated relatively recently in the thymus, preferentially migrating into spleen and there becoming resistant to tolerance induction.
Membrane ionic currents were measured in pregnant rat uterine smooth muscle under voltage clamp conditions by utilizing the double sucrose gap method, and the effects of conditioning pre-pulses on these currents were investigated. With depolarizing pulses, the early inward current was followed by a late outward current. Cobalt (1 mM) abolished the inward current and did not affect the late outward current per se, but produced changes in the current pattern, suggesting that the inward current overlaps with the initial part of the late outward current. After correction for this overlap, the inward current reached is maximum at about +10 mV and its reversal potential was estimated to be +62 mV. Tetraethylammonium (TEA) suppressed the outward currents and increased the apparent inward current. The increase in the inward current by TEA thus could be due to a suppression of the outward current. The reversal potential for the outward current was estimated to be -87 mV. Conditioning depolarization and hyperpolarization both produced a decrease in the inward current. Complete depolarization block occurred at membrane potential of -20 mV. Conditioning hyperpolarization experiments in the presence of cobalt and/or TEA revealed that the decrease in the inward current caused by conditioning hyperpolarization was a result of an increase in the outward current overlaping with the inward current. It appears that a part of the potassium channel population is inactivated at the resting membrane potential and that this inactivation is removed by hyperpolarization.
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Acetylcholine (ACh) levels in whole brains or discrete areas of mice brains were measured after sacrificing by decapitation, conventional or high-powered microwave irradiation. ACh levels in mice brains varied according to the time required to inactivate the enzymes. ACh levels after high-powered microwave irradiation for a shorter time were significantly higher than those after conventional irradiation.
The distribution of the indoleamine 2,3-dioxygenase activity was investigated in various parts of the rabbit brain using the supernatant fraction (30,000 X g, 30 min) of homogenates. A low but significant activity was detected in all parts of the brain. The highest activity was associated with the pineal gland and choroid plexus. Specific activities of the supernatant fractions derived from the pineal gland and choroid plexus were 84.8 and 34.2 pmol/h/mg of protein at 37 degrees C, respectively, with L-tryptophan as substrate. When the pineal gland was cultured with L-[methylene-14C]tryptophan, L-[methylene-14C]kynurenine formed by the action of indoleamine 2,3-dioxygenase was found as one of the major products. It was isolated by DEAE-cellulose column chromatography and identified by thin layer chromatography with and without the treatment by kynureninase from a pseudomonad. The amount of kynurenine thus measured accounted for approximately one-third of the total amount of tryptophan metabolites, indicating that the kynurenine pathway is one of the major metabolic pathways of tryptophan in the rabbit pineal gland.
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A water-soluble phosphate ester of delta8-tetrahydrocannabinol (delta8-THC) was synthesized and its pharmacological activities were examined. The cataleptogenic and thiopental sleep-potentiating effects of delta8-THC phosphate in the mouse was approximately 10 and 7% of those of delta8-THC, respectively. However this phosphate showed almost the same potency and a longer duration of hypothermic effect, as compared with delta8-THC in the mouse. The acute toxicity of this phosphate was far lower than that of delta8-THC. delta 8-THC phosphate was difficultly hydrolyzed by alkaline phosphatase or mouse liver homogenate in vitro. The mode of action of the phosphate derivative is discussed in connection with this enzymatically difficult hydrolysis.
The oral administration of N,'N-2,7-fluorenylenebis-acetamide (2,7-FAA) induces leukemia, especially mature granulocytic leukemia in rats. We compared the degree of infiltration of 2,7-FAA-induced mature granulocytic leukemia with that of transplanted leukemia for the purpose of proving hematogenous development of leukemia. The bone marrow, spleen and liver were examined in the cases of diffuse lesion of 2,7-FAA-induced and transplanted leukemia. The average degree of infiltration of both 2,7-FAA-induced and transplanted leukemia was high in the bone marrow, medium in the spleen, and low in the liver. Intravenous transplantation of malignant neoplasm is an example of hematogenous metastasis. The similarity of infiltration between 2,7-FAA-induced and transplanted leukemia suggests that the former is spread by hematogenous metastasis.
Oral administration of N,N'-2,7-fluorenylenebis-acetamide (2,7-FAA) induces mature granulocytic and erythroblastic leukemia in rats. We compared the primary site of mature granulocytic leukemia with that of erythroblastic leukemia. The nodular foci of solitary lesions and comspicuously large foci of scattered lesions were considered to be the primary site. They appeared mainly in the bone marrow of various bones. The primary site of mature granulocytic leukemia appeared more frequently in short bones than in long bones. On the contrary, that of erythroblastic leukemia appeared more frequently in long bones than in short bones. The origin of mature granulocytic leukemia seems to be concerned with bone tissue, while erythroblastic leukemia may have little relation with bone tissue.
The oral administration of N,N'-2,7-fluorenylenebisacetamide (2,7-FAA) induces leukemia, especially mature granulocytic leukemia, in rats. We compared the distribution of nodular foci of 2,7-FAA-induced mature granulocytic leukemia with that of transplanted leukemia for the purpose of proving hematogenous development of leukemia. The bone marrow of the vertebral bodies was examined in the cases of scattered lesion of 2,7-FAA-induced and transplanted leukemia. The leukemic nodular foci were most frequently located around the center of the craniocaudal axis of the vertebral bodies in both leukemias. On the other hand, they were evenly distributed along the dorso-ventral axis in both leukemias. The similarity of the distribution of nodular foci between 2,7-FAA-induced and transplanted leukemia may be an evidence for the hypothesis that the former is spread by hematogenous metastasis.
1 In rabbit isolated thoracic aortae, effects of magnesium ions on the contraction and (3)H-efflux in response to electrical transmural stimulation and on the contractile responses induced by noradrenaline and KCl were investigated.2 Addition of magnesium (1.2, 3.6, 12.0 and 24.0 mM) to the bathing solution inhibited the electrically induced contractions in a dose-related manner; the inhibition was complete with a concentration of 24.0 mM.3 The increase in (3)H-efflux induced by electrical transmural stimulation was inhibited by the addition of magnesium to the superfusing fluid, but a complete block was not obtained even in high concentrations of magnesium.4 Magnesium ions (1.2, 3.6, 12.0 and 24.0 mM) inhibited the contractile responses induced by low concentrations of noradrenaline (2 x 10(-8)M) and KCl (2 x 10(-2)M). However, the responses induced by higher concentrations of noradrenaline (5 x 10(-7) and 10(-5)M) and KCl (3 and 4 x 10(-2)M) were enhanced by low concentrations of magnesium.5 Magnesium ions affect both presynaptic and effector sites in rabbit thoracic aortae but in a different manner; magnesium manifests only an inhibitory effect on noradrenaline release from the adrenergic nerves, but dual effects on reactivity of vascular smooth muscle, depending on concentrations of magnesium and stimulants; it is suggested that the change in vascular reactivity is more important than the reduction in transmitter release when magnesium inhibits the response to nerve stimulation.